Figure 1.

The molecular pathogenesis of thyroid cancer involves dysregulation of the mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3 kinase (PI3K)/AKT pathways. Common activating mutations in the MAPK pathway include RET-PTC and NTRK rearrangements, and RAS and BRAF mutations. Common genetic alterations in the PI3K pathway include RAS mutations, PTEN mutations or deletions, PIK3K mutations or amplifications, and AKT1 mutations. PAX8-PPARG fusions are common in FTC. Activation of Wnt/b-catenin pathway, inactivating mutations in TP53, and activating mutations in TERT promoter are frequent in undifferentiated thyroid cancer.